1. Technical Field of the Invention
The present invention relates to a method of producing a therapeutic agent for use in the prevention of cancer that arises from mutations to the BRCA1 and BRCA2 genes, i.e., breast and ovarian, and the treatment of several types of human diseases including, but not limited to, Antiphospholipid Syndrome, Disseminate Intravascular Coagulation (DIC), infections arising from viruses (including strains of Human Papillomavirus (HPV), Herpes Simplex Virus (HSV), Simian Virus (SV), tuberculosis (including XDR Tuberculosis) and mycoplasma, Hepatitis A, B and C, MTHFR genetic mutations.
The agent works at the cellular level. In some cases it enables cells to mount an effective defense against infectious agents and has also effected the restoration of proper protein morphology, protein folding, and epigenetic signaling for damaged BRCA1, BRCA2 and MTHFR genes. In other cases, it acts to prevent BRCA1 and BRCA2 mutations from developing oncogenic cells. This represents an entirely new front in the battle against BRCA1 and BRCA2 related cancers.
The technical field of the invention is a formulation that acts on human cells with nutraceutical, pharmaceutical, genetic repair and epigenetic repair modes of action.
2. Description of the Related Art
A variety of therapeutic agents have been employed to treat or prevent the conditions cited above. Some attack invasive or infectious microbes while some directly attack diseased human cells. These agents often require complex synthesis methods or have a risky dosing scheme and method of administration. Still, few of these agents are effective and fewer act at the cellular level in a manner that enables them to break biofilms or mount an effective counterattack to these invaders or to correct any related genetic mutations.
The field of epigenetics is now key in the research and development of therapies to address pathology in the cells of living organisms. Great strides have been made now that we have an increased understanding of various epigenetic mechanisms, like histone modification, DNA methylation and small non-coding RNAs.
Research has documented that mutations affecting the DNA Damage Recovery Pathways often lead to mutations in genes as well as to alterations in epigenetic signaling of genes including BRCA1, BRCA2 and MTHFR. Together, these mutations and signaling abnormalities turn off apoptosis signals or turn on senescence signals that leave these cells susceptible to mutation, infection, and toxins. Current genetic scanning technology detects these cellular conditions as abnormal gene sequences, single nucleotide polymorphisms, abnormal morphologies and abnormal protein folding patterns.
In some cases these mutations are somatic cell abnormalities only, and their resolution resolves the present disease condition. However, some mutations are germ-line mutations that, if not corrected, will be inherited by future generations.
In the case of viral infections, many attempts have been made at producing vaccines, with limited success. In the case of HPV, HSV, SV and viral Hepatitis, few agents are effective at halting the progression of an active infection and none are known to succeed at destroying the virus in the cell.
Carnitine plays a key role in fatty acid oxidation. Because of this role, there is interest as to whether carnitine D-Boramine has been proven to be beneficial in genetic or acquired disorders of energy production to improve fatty acid oxidation, to remove accumulated toxic fatty acyl-CoA metabolites, or to restore the balance between free and acyl-CoA. There are two known disorders in children where the carnitine supply becomes limiting for fatty acid oxidation, and supplementation with carnitine is essential. The first disorder is a recessive genetic defect of the muscle/kidney sodium-dependent, plasma membrane carnitine transporter, which presents as cardiomyopathy or hypoketotic hypoglycemia in infancy. The second disorder arises from chronic administration of pivalate conjugated antibiotics, in which excretion of pivaloyl-carnitine can result in carnitine depletion. In the latter situation, tissue levels may become low enough to limit fatty acid oxidation. The benefits of carnitine supplementation in secondary carnitine deficiencies may require invasive endurance studies of fasting ketogenesis or muscle and cardiovascular work, as carnitine becomes rate limiting only at very low concentrations.
Hence there is a need to develop a therapeutic agent that is effective in the prevention of cancers arising from BRCA1 and BRCA2 genetic mutations, and in the treatment of viral infections, cancers, tuberculosis, and other diseases, and to repair disorders arising from carnitine deficiency. There is a need to provide a therapeutic agent that can enter both somatic and germ-line cells, and enable the mitochondria to repair these defects and restore a non-mutated homeostasis to the cell and its intra-cellular signaling.
There is also a need to come up with a simple method of preparing a therapeutic agent and administering it.
The above-mentioned shortcomings, disadvantages and problems are addressed herein as detailed below.